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Mod GRF 1-29 (CJC-1295 NO DAC) (5mg)
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What is the Mod GRF (1-29) Peptide?
Mod GRF (1-29) is a synthetic peptide analog of growth hormone-releasing hormone (GHRH). It was first developed in the 1980s when studies revealed that the first 29 amino acids of GHRH possessed all of the biological roles associated with the full-length 44 residue protein. The initially designed peptide, known as GRF (1-29), is the shortest segment of GHRH, and appears to possess all the properties of the full-length hormone. A different truncated synthetic form of GHRH known as Sermorelin or GRF 1-29 also has 29 amino acids. Modified GRF (1-29) undergoes alteration to include four substituted amino groups in its chain. The intention behind these amino modifications is to protect the peptide from both oxidation and degradation during manufacture and transport and in vivo. The modification also appears to increase the binding affinity to GHRH receptors. Though GRF happens to be biologically potent like GHRH, the duration of action is restricted due to a short half-life (less than 10 minutes). As a result, researchers have modified it hoping to enhance its half-life with better therapeutic potential. Modified GRF (1-29) is also known as Mod GRF or Tetra-substituted GRF (1-29). The latter name clarifies that the modified peptide differs from GRF (1-29) as a result of changes in four of its amino acids. Modified GRF (1-29) is identical to CJC-1295 without DAC.
AKA: Mod GRF (1-29)
Molecular Formula: C152H252N44O42
Molecular Weight: 3367.95 g/mol
PubChem: CID 56841945
CAS Number: 863288-34-0
Mod GRF (1-29) Research
Modified GRF has been studied for its potential to mediate the same biological effects as GHRH, including muscle growth (hypertrophy), improved bone development, enhanced lipolysis, accelerated metabolism, and wound healing. It also may positively influence the immune system and blood sugar regulation.
Modified GRF 1-29 and Cardiac Function
Research in rodent models has observed that modified GRF and other GHRH derivatives may improve the capacity of the heart to pump blood even after a heart attack. More specifically, the researchers comment that “Various studies demonstrate that GHRH agonists promote repair of cardiac tissue, producing improvement of ejection fraction and reduction of infarct size in rats, reduction of infarct scar in swine, and attenuation of cardiac hypertrophy in mice.” This could be of immense potential in improving the quality of life and reducing death over the long term in patients diagnosed with cardiac failure. Modified GRF has the potential to be effective in the treatment of pulmonary hypertension, cardiac failure, heart attack, and diverse congenital heart conditions.
Modified GRF 1-29 and the Intestine
Early studies have highlighted that growth hormone (GH) may be beneficial for Crohn’s disease, short bowel syndrome, and other inflammatory bowel conditions. Unfortunately, the adverse effects of long-term use exceed the benefits of the hormone. Thus, researchers have looked into GHRH analogs for mediating a similar effect. Research in monkeys suggested that Mod GRF 1-29 binds with vasoactive intestinal peptide (VIP) receptors and improves bowel motility, as improved bowel movement is crucial in inflammatory bowel diseases associated with constipation. The peptide appears to interact with VIPC1, present on the smooth muscle of the reproductive, gastrointestinal as well as urinary systems.  These conditions trigger a great deal of morbidity and are difficult to address due to the lack of alternative drug options.
Mod GRF 1-29 and Thyroid, Growth Hormone
Malfunctioning of the thyroid gland is often associated with concomitant issues in GH release. Research studies have suggested that individuals who suffer from hyperthyroidism and receive the thyroid replacement hormone demonstrate stronger reactions to GRF, providing a possible a link between thyroid hormone and GH. The scientists commented that “These data indicate that thyroid hormone […] enhances the responsiveness of the somatotroph to GRF 1-29.” Thus, peptides like Modified GRF may contribute towards a better understanding of human physiology. Experimental studies in Modified GRF 1-29 note that the peptide appears to exhibit mild side effects, low oral bioavailability, and excellent subcutaneous bioavailability in mice. The dosage required in mice (per kg) does not scale to that suitable for humans.
- Cen, L. P., Ng, T. K., Chu, W. K., & Pang, C. P. (2022). Growth hormone-releasing hormone receptor signaling in experimental ocular inflammation and neuroprotection. Neural regeneration research, 17(12), 2643–2648. https://doi.org/10.4103/1673-5374.336135
- Jetté, L., Léger, R., Thibaudeau, K., Benquet, C., Robitaille, M., Pellerin, I., Paradis, V., van Wyk, P., Pham, K., & Bridon, D. P. (2005). Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology, 146(7), 3052–3058. https://doi.org/10.1210/en.2004-1286
- Schally, A. V., Zhang, X., Cai, R., Hare, J. M., Granata, R., & Bartoli, M. (2019). Actions and Potential Therapeutic Applications of Growth Hormone-Releasing Hormone Agonists. Endocrinology, 160(7), 1600–1612. https://doi.org/10.1210/en.2019-00111
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- Waelbroeck, M., Robberecht, P., Coy, D. H., Camus, J. C., De Neef, P., & Christophe, J. (1985). Interaction of growth hormone-releasing factor (GRF) and 14 GRF analogs with vasoactive intestinal peptide (VIP) receptors of rat pancreas. Discovery of (N-Ac-Tyr1,D-Phe2)-GRF(1-29)-NH2 as a VIP antagonist. Endocrinology, 116(6), 2643–2649. https://doi.org/10.1210/endo-116-6-2643
- Valcavi, R., Jordan, V., Dieguez, C., John, R., Manicardi, E., Portioli, I., Rodriguez-Arnao, M. D., Gomez-Pan, A., Hall, R., & Scanlon, M. F. (1986). Growth hormone responses to GRF 1-29 in patients with primary hypothyroidism before and during replacement therapy with thyroxine. Clinical endocrinology, 24(6), 693–698. https://doi.org/10.1111/j.1365-2265.1986.tb01666.x
Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.